A unifying model of the immunoregulatory role of the interferon system: can interferon produce disease in humans?

Abstract

This hypothesis is a presentation of a unifying model of the interferon (IFN) system as a cascade of sequentially interacting responses of IFNs-alpha, -beta, and -gamma involved in modulation of the immune response. We propose that every antigen is an IFNogen. The first stage(s) of immune responsiveness is associated primarily with the production of the family of IFN-alpha. In certain immunologically mediated diseases, including the autoimmune diseases and AIDS, disturbances in the synthesis of IFN-alpha occur with a switch to the production of predominantly acid-labile types, which have a negative immunoregulatory effect. Moreover, disturbances of IFN synthesis in the embryo or fetus can lead to deformities. Some viruses and other biological and chemical substances manifest a pathological effect by the IFN they induce. This IFN may help sustain the viruses and other substances which induce this IFN. We think it is unsafe to give patients immunoregulators in incomplete form. Thus, there is a potential danger in giving patients recombinant forms of IFNs and interleukin 2 produced in bacteria. In certain immune disorders, we may be able to treat patients by the binding or removal of hyperproduced IFNs from the body. This may lead to the restoration of immunologic balance and clinical improvement.